Concussion is one of the most commonly misunderstood injuries in medicine. It is frequently described as a “mild brain injury” — which is technically accurate and substantially misleading at the same time.
What’s actually happening in the brain
A concussion occurs when the brain undergoes rapid acceleration-deceleration, typically from a blow to the head or a whiplash force. The brain is not a rigid structure fixed in place — it is a soft tissue suspended in cerebrospinal fluid inside the skull. When the head decelerates rapidly, the brain continues moving briefly, distorting and stretching neural tissue.
The primary injury is not structural in the way a bruise or cut is. Imaging in uncomplicated concussion — CT or MRI — usually appears normal. The injury is functional: the mechanical deformation of neurons triggers an ionic cascade. Potassium floods out of neurons, sodium and calcium flood in, glutamate (an excitatory neurotransmitter) is released in excess. The brain responds by sharply increasing glucose consumption to restore ionic balance — while simultaneously reducing cerebral blood flow.
The result is an energy crisis in the brain: high metabolic demand and reduced blood supply occurring at the same time. This is what produces the symptoms.
The symptom picture
Concussion can produce headache, dizziness, nausea, sensitivity to light and noise, cognitive slowing, and sleep disturbance. In most people, these resolve within 7–14 days as the ionic environment normalises and metabolism returns to baseline.
In around 20–30% of cases, symptoms persist beyond this period — a condition called post-concussion syndrome. Its mechanisms are less well understood and its management remains largely symptomatic.
Why repeated concussions are different
The acute energy crisis of a single concussion is usually survivable without lasting damage. The concern with repeated concussions is different: evidence accumulated over the past two decades has linked repeated traumatic brain injury — particularly in contact sports — to a degenerative condition called chronic traumatic encephalopathy (CTE).
CTE involves accumulation of tau protein in the brain, producing progressive cognitive impairment, mood disturbance, and behavioural changes years or decades after the original injuries. It has been identified post-mortem in former American football players, boxers, and rugby players. The minimum number of concussions required to produce CTE is unknown, and CTE currently cannot be diagnosed in a living patient — only by post-mortem brain examination.
The “return to play” problem
The window immediately after a concussion, when the brain is in its energy crisis phase, is a period of particular vulnerability. A second impact during this period — before full recovery — produces disproportionately worse injury, a phenomenon called second impact syndrome. This is why return-to-play protocols in sport are not conservative overcaution: they reflect real evidence of accelerated pathology in the vulnerable period.
The word “mild” in “mild traumatic brain injury” refers to the absence of structural damage and the usual resolution of symptoms, not to the seriousness of the mechanism.